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IL6/JAK/STAT3-mediated crosstalk between cancer associated fibroblasts and epithelial cells promotes lineage plasticity and prostate cancer progression [scATAC-seq]

ABSTRACT: IL6/JAK/STAT3-mediated crosstalk between cancer associated fibroblasts and epithelial cells promotes lineage plasticity and prostate cancer progression [scATAC-seq]

PROVIDER: PRJNA988486 | ENA |

REPOSITORIES: ENA

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IL6/JAK/STAT3-mediated crosstalk between cancer associated fibroblasts and epithelial cells promotes lineage plasticity and prostate cancer progression [scATAC-seq]

Project description:Prostate cancer is a heterogeneous disease with a slow progression and a highly variable clinical outcome. The tumor suppressor gene TP53 is frequently mutated in prostate cancer and predictive of an early metastatic dissemination and unfavorable patient outcome. The progression of solid tumors to metastatic cancer is often associated with increased cell plasticity, but the mechanism underlying TP53-loss induced disease aggressiveness is unknown. Here we show that Trp53 deficiency in Pten-null prostatic epithelial cells does not impact the early proliferation of Pten-null epithelial cells and prostatic intraepithelial neoplasia formation, nor growth arrest and senescence entry at later time. Moreover, we demonstrate that it induces epithelial cell plasticity by stimulating IL6 production in cancer-associated fibroblasts, that in turn enhances Jak/Stat signaling in epithelial cells and promotes metastatic dissemination. Thus, TP53 restrains prostate cancer progression by preventing a pro-tumorigenic crosstalk between PTEN-deficient prostatic epithelial cells and the tumor microenvironment.

2025-02-05 | GSE236040 | GEO

IL6/JAK/STAT3-mediated crosstalk between cancer associated fibroblasts and epithelial cells promotes lineage plasticity and prostate cancer progression [scRNA-seq]

2025-02-05 | GSE236041 | GEO

IL6/JAK/STAT3-mediated crosstalk between cancer associated fibroblasts and epithelial cells promotes lineage plasticity and prostate cancer progression.

Project description:IL6/JAK/STAT3-mediated crosstalk between cancer associated fibroblasts and epithelial cells promotes lineage plasticity and prostate cancer progression.

| PRJNA988480 | ENA

IL6/STAT3 co-opts ER regulatory elements to drive metastasis in breast cancer

Project description:Interleukin 6 (IL6) signaling has been associated with an aggressive and metastatic phenotype in multiple solid tumors including breast cancer, but its mechanism of action in mediating tumor progression and treatment response is not clear. By exploiting a clinically relevant intraductal xenograft model of estrogen receptor positive (ER+) breast cancer, we demonstrate that IL6 increases both primary tumor growth and distant metastases. By integrating pre-clinical models and clinical specimens, we show that signal transducer and activator of transcription 3 (STAT3) mediates IL6-induced activation of a metastatic gene program from enhancer-elements shared with ER and its pioneer factor FOXA1. Although IL6 activated STAT3 and ER/FOXA1 share cis-regulatory regions, STAT3 drives transcription independent of ER and FOXA1 function, and the IL6/STAT3 gene program is not influenced by ER-targeted therapies, decoupling these two important pathways. This demonstrates that ER/FOXA1 and IL6/STAT3 are two parallel, but independent actionable pathways controlling breast cancer progression.

2021-09-08 | PXD012980 | Pride

IL6/JAK/STAT3-mediated crosstalk between cancer associated fibroblasts and epithelial cells promotes lineage plasticity and prostate cancer progression [scRNA-seq]

Project description:IL6/JAK/STAT3-mediated crosstalk between cancer associated fibroblasts and epithelial cells promotes lineage plasticity and prostate cancer progression [scRNA-seq]

| PRJNA988485 | ENA

Increased risk of mammary cancer recurrence in socially isolated rats is linked to upregulation of IL6/JAK/STAT3 and inhibition of oxidative phosphorylation signaling, activities blocked by the herbal mixture Jaeumganghwa-tang

Project description:While multifactorial in origin, one of the most prevalent and impactful consequences of social isolation is an increase in cancer mortality. Using a preclinical model in Sprague Dawley rats, we found that social isolation increased the risk of mammary tumor recurrence after completion of antiestrogen therapy. The increased recurrence risk was associated with an upregulation of IL6/JAK/STAT3 signaling in the mammary glands and tumors and suppression of mitochondrial oxidative phosphorylation (OXPHOS) pathway. Also inhibited were genes involved in mitochondrial pyruvate transport and the conversion of pyruvate to acetyl CoA but lactate levels were not altered. In addition, social isolation increased the expression of receptor for advanced glycation end-products (RAGE), consistent with the impaired insulin sensitivity and weight gain linked to social isolation. All these changes are commonly associated with aging. In socially isolated animals consumption of the anti-inflammatory 12 herb mixture Jaeumganghwa-tang (JGT) inhibited IL6/JAK/STAT3 signaling, upregulated OXPHOS signaling, suppressed expression of the RAGE ligands S100a8 and S100a9, and prevented the increased risk of mammary cancer recurrence. In summary, increased breast cancer mortality among socially isolated survivors may be most effectively prevented by focusing on the period following the completion of endocrine therapy using tools that inhibit IL6/JAK/STAT3 inflammatory cytokine signaling and reverse disrupted OXPHOS.

2023-04-18 | GSE201117 | GEO

An IL6-STAT3-MR-FGF21 Axis Mediates Heart-Liver Crosstalk after Myocardial Infarction

Project description:The liver plays a protective role in myocardial infarction (MI). However, very little is known about the mechanisms. Here, we identify mineralocorticoid receptor (MR) as a pivotal nexus that conveys communications between the liver and the heart during MI. On one hand, hepatocyte MR deficiency and MR antagonist spironolactone both improve cardiac repair after MI through regulation on hepatic fibroblast growth factor 21 (FGF21), illustrating an MR/FGF21 axis that underlies the liver-to-heart protection against MI. On the other hand, an upstreaming acute interleukin-6 (IL6) / signal transducer and activator of transcription 3 (STAT3) pathway transmits the heart-to-liver signal to suppress MR expression after MI. Hepatocyte IL6 receptor (IL6R) deficiency and STAT3 deficiency both aggravate cardiac injury through their regulation on the MR/FGF21 axis. Therefore, we have unveiled an IL6/STAT3/MR/FGF21 signaling axis that mediates heart-liver crosstalk during MI. Targeting the signaling axis and the crosstalk may provide novel strategies to treat MI and heart failure.

2023-01-01 | GSE193516 | GEO

IL6/STAT3 co-opts ER/FOXA1 regulatory elements to drive metastasis in breast cancer [ATAC-Seq]

2020-07-17 | GSE150131 | GEO

IL6/STAT3 co-opts ER/FOXA1 regulatory elements to drive metastasis in breast cancer (ChIP-Seq)

2020-07-17 | GSE126004 | GEO

N-Glycosylation-Defective IL6 Alternatively Activates the SRC-YAP-SOX2 Axis to Drive Metastasis and EGFR TKI Resistance

Project description:The IL6-GP130-STAT3 pathway facilitates lung cancer progression and resistance to tyrosine kinase inhibitors. Although glycosylation alters the stability of GP130, its effect on the ligand IL6 remains unclear. We herein found that N-glycosylated IL6, especially at Asn73, primarily stimulates JAK-STAT3 signaling and prolongs STAT3 phosphorylation, whereas N-glycosylation-defective IL6 (deNG-IL6) induces shortened STAT3 activation and alters the downstream signaling preference for the SRC-YAP-SOX2 axis. This signaling shift induced EMT and migration in vitro and metastasis in vivo, which were suppressed by targeted inhibitors and shRNAs against SRC, YAP, and SOX2. Osimertinib-resistant lung cancer cells secreted a large amount of deNG-IL6 through reduced N-glycosyltransferase gene expression, leading to clear SRC-YAP activation. deNG-IL6 contributes to drug resistance, as confirmed by in silico analysis of cellular and clinical transcriptomes and signal expression in patient specimens. Therefore, the N-glycosylation status of IL6 not only affects cell behaviors but also shows promise in monitoring the dynamics of lung cancer evolution.

2025-01-18 | PXD051771 | Pride

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